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• W2002771345 abstract "Chronic hepatitis C infection persists in more than 170 million people worldwide and is one of the major causes of hepatic failure and liver transplantation. Recent studies have demonstrated that hepatitis C virus (HCV)-derived proteins have the capacity to generate substantial oxidative stress within the hepatocyte. Subsequently, oxidative stress has been identified as a significant mechanistic pathway culminating in the development of hepatic cirrhosis, liver failure and liver cancer. In vitro HCV-induced oxidative stress has been demonstrated to activate cellular signaling pathways involved in both inflammatory and fibrogenic responses. In addition, oxidative stress has also been shown to play a role in HCV replication. Preliminary data from small clinical trials have implicated oxidative stress as a risk factor for liver fibrosis and increased HCV viral load. Although conclusive evidence from large-scale clinical trials is lacking, it is possible that antioxidant co-therapies may improve hepatic inflammation, retard fibrosis progression and improve the ability to achieve a sustained viral response with standard antiviral therapy." @default.
• W2002771345 created "2016-06-24" @default.
• W2002771345 creator A5013770831 @default.
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• W2002771345 date "2006-03-01" @default.
• W2002771345 modified "2023-09-26" @default.
• W2002771345 title "Hepatitis C virus and oxidative stress: a dangerous liaison" @default.
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• W2002771345 doi "https://doi.org/10.2217/17460794.1.2.223" @default.
• W2002771345 hasPublicationYear "2006" @default.
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